BERKELEY <\/p>\n
Some 10 percent of the population suffers from eczema at some point in their lives. The chronic skin condition, for which there are no cures or good treatments, causes symptoms ranging from dry, flaky and itchy skin to flaming red rashes and, particularly in children, nasal allergies and asthma. <\/p>\n
Scientists at the University of California, Berkeley, have developed a new picture of how the nervous system interacts with the immune system to cause the itch and inflammation associated with eczema. Their findings could lead to new therapies for the disease. <\/p>\n
Eczemas cause is unknown, but most research today focuses on the immune systems role in reacting to chemicals that cause itching and inflammation. UC Berkeley neuroscientist Diana M. Bautista and graduate students Sarah R. Wilson and Lydia Th, however, discovered that sensory nerves in the skin are the first to react to these chemicals, and that blocking the skins itch receptors not only stops the scratching, but may head off the worst consequences of eczema. <\/p>\n
Most drug development has focused on trying to find a way to inhibit the immune response, said Bautista, assistant professor of molecular and cell biology and a member of the Helen Wills Neuroscience Institute. Now that we have found that sensory neurons may be the first responders, that changes how we think about the disease. <\/p>\n
By just blocking what is happening in the neurons, you could block the symptoms of chronic itch, including the big immune response leading to asthma and allergy, Wilson added. And you prevent the patient from scratching, which damages skin cells and makes them release more chemicals that cause inflammation and help maintain chronic itch. <\/p>\n
The researchers already have identified a potential drug, now in Phase 1 clinical trials for a different inflammatory disease, that stops mice from scratching when it is applied to the skin. <\/p>\n
Their new model of eczema is based on findings reported online today (Thursday, Oct. 3) in the journal Cell by Bautista, Wilson, Th and their UC Berkeley colleagues. <\/p>\n
Block that wasabi We started out looking at acute itch and asked the question, Why do we scratch? Why do we have that urge, and how does it work that scratching gives you some relief, when normally it feels terrible if you dont have an itch and scratch yourself that hard? Bautista said. But the many types of chronic itch that humans experience are all very different. We believe that, through identifying molecular mechanisms, we can find new treatments and therapies for these diseases. <\/p>\n
Immunologists several years ago identified a chemical TSLP (thymic stromal lymphopoietin), a so-called cytokine that induces itch when expressed in the skin. Because immune cells have receptors for this chemical, TSLP triggers them to release chemicals that attract other immune cells and to create the red, itchy inflammation typical of eczema. These inflammatory chemicals seem to spread through the body and induce inflammation in the lungs, gut and nasal passages that lead to asthma and allergies, Bautista said. <\/p>\n
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Read more: BERKELEY Some 10 percent of the population suffers from eczema at some point in their lives. The chronic skin condition, for which there are no cures or good treatments, causes symptoms ranging from dry, flaky and itchy skin to flaming red rashes and, particularly in children, nasal allergies and asthma. Scientists at the University of California, Berkeley, have developed a new picture of how the nervous system interacts with the immune system to cause the itch and inflammation associated with eczema. Continue reading
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